Mechanism Of Ventricular Tachycardia Research Articles

Prediction of self-terminating Ventricular Tachycardia in isolated rat heart experiments by using wavelet analysis

This study investigates whether self-terminating and prolonged ventricular tachycardias (VT) can be differentiated using cross-wavelet analysis. VT is a type of arrhythmia that may persist or transform into other arrhythmias. In this study, 40 VT samples from 7 isolated rat hearts are analyzed, including 19 prolonged VTs and 21 self-terminating VTs (STVTs). Bivariate timeseries of left ventricular and right atrium are analyzed using cross-wavelet analysis to find correlations between the signals. The results show that self-terminating VT occurs most frequently when there is a weak correlation between the signals, while prolonged VT is associated with a strong correlation between ventricular and atrial signals. The study suggests that mechano-electrical interaction between the right atrium and left ventricle may be the underlying mechanism for this connection. The findings may have implications for understanding the underlined mechanism and treatment of VT in clinical practice.

Multi-Faceted Approach to Ventricular Tachycardia: A Review of Management Strategies

Ventricular tachycardia poses a significant therapeutic challenge. It can manifest over a spectrum from minimal palpitation symptoms to sudden cardiac death. This makes large-scale trials on the treatment of ventricular tachycardia difficult to perform. The mechanism of ventricular tachycardia must also be understood before embarking on treatment. Patients with or without structural heart disease will have different mechanisms for the onset and propagation of these arrhythmias. Catheter ablation is an established management option for ventricular tachycardia; however, it is not always successful and anti-arrhythmic medications are often necessary to control these life-threatening arrhythmias. Although anti-arrhythmics can suppress ventricular tachycardias they also carry side effects. In certain substrates, some of these medications can exacerbate arrhythmias or heart failure. For these reasons, a multifaceted approach to treating ventricular tachycardia is necessary. This paper is a comprehensive review of the comprehensive management strategies for ventricular tachycardia. Anti-arrhythmic medications have an important role and their use in various cardiomyopathies and channelopathies is reviewed in detail. We also review the promising effects of gene therapy and artificial intelligence on different substrates for ventricular tachycardia.

Characterization of ventricular tachycardia ablation in end-stage heart failure patients with left ventricular assist device (CHANNELED-Registry)

Abstract Background Left-ventricular-assist-devices (LVAD) are an established therapy for patients with end-stage heart failure. These patients are at high risk for ventricular tachycardia (VT) and ICD-shocks due to the arrhythmogenic substrate of the underlying cardiomyopathy itself and as the LVAD cannula might be arrhythmogenic, too. Purpose Data on catheter ablation of VT in LVAD patients are scarce and current evidence predominantly consists of case reports and small single-center series. This multicenter registry seeks to systematically assess the mechanism and origin of VA in LVAD patients and to evaluate procedural parameters and outcome of VT ablation in this special subset of patients. Methods Retrospective data of LVAD patients referred for VT ablation at 11 tertiary care centers between January 2017 and August 2023 were included in this multicenter registry. VT mechanisms, procedural data, clinical follow-up, and outcome were assessed. Results We report 49 patients (88% male, age 61±8 years) undergoing 51 ablation procedures included in this ongoing registry. The underlying cardiomyopathy was ischemic in 25/49 patients (51%) and nonischemic in 24/49 patients (49%) with a mean left ventricular ejection fraction of 21%±6% before LVAD implantation. Most catheter ablations were conducted after prior antiarrhythmic drug (AAD) treatment (15/51 on amiodarone, 13/51 on prior intensification of amiodarone treatment, 18/51 on prior combination of two or more AADs). A total of 75 VTs were targeted (39/51 transseptal, 3/51 retrograde aortic, 9/51 combined approaches) and 13/49 patients required VT ablation less than 1 month after LVAD implantation. Of the targeted VTs the majority (69%) were cardiomyopathy related and only 31% of the targeted VTs were related to the LVAD cannula. In 5/51 procedures access site complications and in 1/51 procedures a pericardial effusion occurred; one patient showed a post procedural oxygen desaturation; despite immediate intubation the patient deceased from hypoxic brain injury. No LVAD related complications were observed. A follow-up was available for 35/49 patients. During a median follow-up of 277 days (IQR 78-625 days), 5/35 patients were transplanted and 13/35 died. Patients died after a median time of 124 days (IQR 34-952 days) primarily from heart failure, sepsis, or intracranial bleeding. Of the remaining 17/35 patients, 7/17 patients were arrhythmia-free at a median follow-up of 212 days (IQR 78-639 days). Conclusion Although often chosen as last resort, catheter ablation of VT in LVAD patients is feasible and can be performed safely in this critically ill subset of heart failure patients in experienced centers. Intrinsic myocardial scar seems to be the dominant substrate in these patients but LVAD cannulae contribute to a significant number of VTs. In the presence of severely reduced LV function the VT recurrence remains high despite maximal therapy and prognosis of these patients is limited.

Predicting ventricular tachycardia circuits in patients with arrhythmogenic right ventricular cardiomyopathy using genotype-specific heart digital twins.

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic cardiac disease that leads to ventricular tachycardia (VT), a life-threatening heart rhythm disorder. Treating ARVC remains challenging due to the complex underlying arrhythmogenic mechanisms, which involve structural and electrophysiological (EP) remodeling. Here, we developed a novel genotype-specific heart digital twin (Geno-DT) approach to investigate the role of pathophysiological remodeling in sustaining VT reentrant circuits and to predict the VT circuits in ARVC patients of different genotypes. This approach integrates the patient's disease-induced structural remodeling reconstructed from contrast-enhanced magnetic-resonance imaging and genotype-specific cellular EP properties. In our retrospective study of 16 ARVC patients with two genotypes: plakophilin-2 (PKP2, n = 8) and gene-elusive (GE, n = 8), we found that Geno-DT accurately and non-invasively predicted the VT circuit locations for both genotypes (with 100%, 94%, 96% sensitivity, specificity, and accuracy for GE patient group, and 86%, 90%, 89% sensitivity, specificity, and accuracy for PKP2 patient group), when compared to VT circuit locations identified during clinical EP studies. Moreover, our results revealed that the underlying VT mechanisms differ among ARVC genotypes. We determined that in GE patients, fibrotic remodeling is the primary contributor to VT circuits, while in PKP2 patients, slowed conduction velocity and altered restitution properties of cardiac tissue, in addition to the structural substrate, are directly responsible for the formation of VT circuits. Our novel Geno-DT approach has the potential to augment therapeutic precision in the clinical setting and lead to more personalized treatment strategies in ARVC.

Predicting ventricular tachycardia circuits in patients with arrhythmogenic right ventricular cardiomyopathy using genotype-specific heart digital twins

Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a genetic cardiac disease that leads to ventricular tachycardia (VT), a life-threatening heart rhythm disorder. Treating ARVC remains challenging due to the complex underlying arrhythmogenic mechanisms, which involve structural and electrophysiological (EP) remodeling. Here, we developed a novel genotype-specific heart digital twin (Geno-DT) approach to investigate the role of pathophysiological remodeling in sustaining VT reentrant circuits and to predict the VT circuits in ARVC patients of different genotypes. This approach integrates the patient’s disease-induced structural remodeling reconstructed from contrast-enhanced magnetic-resonance imaging and genotype-specific cellular EP properties. In our retrospective study of 16 ARVC patients with two genotypes: plakophilin-2 (PKP2, n = 8) and gene-elusive (GE, n = 8), we found that Geno-DT accurately and non-invasively predicted the VT circuit locations for both genotypes (with 100%, 94%, 96% sensitivity, specificity, and accuracy for GE patient group, and 86%, 90%, 89% sensitivity, specificity, and accuracy for PKP2 patient group), when compared to VT circuit locations identified during clinical EP studies. Moreover, our results revealed that the underlying VT mechanisms differ among ARVC genotypes. We determined that in GE patients, fibrotic remodeling is the primary contributor to VT circuits, while in PKP2 patients, slowed conduction velocity and altered restitution properties of cardiac tissue, in addition to the structural substrate, are directly responsible for the formation of VT circuits. Our novel Geno-DT approach has the potential to augment therapeutic precision in the clinical setting and lead to more personalized treatment strategies in ARVC.

Canine Model of Ischemia-Induced Ventricular Tachycardia

IntroductionDespite advances in antiarrhythmia therapies, ventricular tachycardia (VT) is a leading cause of sudden cardiac death. Investigation into the characteristics and new treatments for this arrhythmia is required to improve outcomes and a reproducible model of VT would be useful in these endeavors. We therefore created a canine model of ischemia-induced VT. Materials and methodsA pacing lead was implanted in the right ventricle in canines (n = 13) and the left anterior descending artery was occluded in two locations for 2 h and subsequently released to create an ischemia-reperfusion injury. In the 10 dogs that survived the first 48 h following the initial study, a terminal study was conducted 4-7 d later and VT was induced using premature stimulation or burst pacing through the right ventricle lead. The arrhythmia was terminated using either antitachycardia pacing or a defibrillatory shock. Multiple inductions into sustained VT were attempted. ResultsSustained VT was induced in eight of 10 dogs with an average cycle length of 335 ± 70 bpm. Multiple episodes of VT were induced. Episodes of VT exhibited different electrocardiogram morphologies and cycle lengths in individual animals. ConclusionsThis canine model provides a consistent technique for inducing multiple episodes of sustained VT. It may be useful for investigating VT mechanisms and testing novel therapeutics and treatments for patients with VT.

The age of computational cardiology and future of long-term ablation target prediction for ventricular tachycardia.

Ventricular arrhythmias, particularly ventricular tachycardia, are ubiquitously linked to 300,000 deaths annually. However, the current interventional procedure-the cardiac ablation-predict only short-term responses to treatment as the heart constantly remodels itself post-arrhythmia. To assist in the design of computational methods which focuses on long-term arrhythmia prediction, this review postulates three interdependent prospectives. The main objective is to propose computational methods for predicting long-term heart response to interventions in ventricular tachycardia Following a general discussion on the importance of devising simulations predicting long-term heart response to interventions, each of the following is discussed: (i) application of "metabolic sink theory" to elucidate the "re-entry" mechanism of ventricular tachycardia; (ii) application of "growth laws" to explain "mechanical load" translation in ventricular tachycardia; (iii) derivation of partial differential equations (PDE) to establish a pipeline to predict long-term clinical outcomes in ventricular tachycardia.

Mechanistic assessment and ablation of left ventricular assist device related ventricular tachycardia in patients with severe heart failure.

Aims: Left-ventricular-assist-devices (lvad) are an established treatment for patients with severe heart failure with reduced ejection fraction (HF) and reduce mortality. However, HF patients have significant substrate for ventricular tachycardia (VT) and the lvad itself might be pro-arrhythmogenic. We investigated the mechanism of VT in lvad-patients in relation to the underlying etiology and provide in silico and ex-vivo data for ablation in these HF patients. Methods and Results: We retrospectively analyzed invasive electrophysiological (EP) studies of 17 patients with VT and lvad. The mechanism of VT was determined using electroanatomical, entrainment and activation time mapping. Ischemic cardiomyopathy was present in 70% of patients. VT originated from the lvad region in >30%. 1/6 patients with VT originating from the lvad region had episodes before lvad implantation, while 7/11 patients with VT originating from other regions had episodes before implantation. Number and time of radiofrequency (RF)-ablation lesions were not different between VTs originating from the lvad or other regions. Long-term freedom from VT was 50% upon ablation in patients with VT originating from the lvad region and 64% if ablation was conducted in other regions. To potentially preemptively mitigate lvad related VT in patients undergoing lvad implantation, we obtained in silico derived data and performed ex-vivo experiments targeting ventricular myocardium. Of the tested settings, application of 25 W for 30s was safe and associated with optimal lesion characteristics. Conclusion: A significant percentage of patients with lvad undergoing VT ablation exhibit arrhythmia originating in close vicinity to the device and recurrence rates are high. Based on in silico and ex-vivo data, we propose individualized RF-ablation in selected patients at risk for/with lvad related VT.

Directed Graph Mapping for Ventricular Tachycardia: A Comparison to Established Mapping Techniques

BackgroundUnderstanding underlying mechanism(s) and identifying critical circuit components are fundamental to successful ventricular tachycardia (VT) ablation. Directed graph mapping (DGM) offers a novel technique to identify the mechanism and critical components of a VT circuit. ObjectivesThis study sought to evaluate the accuracy of DGM in VT ablation compared with traditional mapping techniques and a commercially available automated conduction velocity mapping (ACVM) tool. MethodsPatients with structural heart disease who had undergone a VT ablation with entrainment-proven critical isthmus and a high-density electroanatomical activation map were included. Traditional mapping (TM) consisted of a combination of local activation time and entrainment mapping and was considered the gold standard for determining the VT mechanism, circuit, and isthmus location. The same local activation time values were then processed using DGM and a commercially available ACVM (Coherent Mapping, Biosense Webster) tool. The aim of this study was to compare TM vs DGM and ACVM in their ability to identify the VT mechanism, characterize the VT circuit, and locate the critical isthmus. ResultsThirty-five cases were identified. TM classified the VT mechanism as focal in 7 patients and re-entrant in 28 patients. TM classified 11 VTs as single-loop re-entry, 15 as dual-loop re-entry, 1 as complex, and 1 case was indeterminant. The overall agreement between DGM and TM for determining VT mechanism and circuit type was strong (kappa value = 0.79; P < 0.01), as was the agreement between ACVM and TM (kappa value = 0.66; P < 0.01). Both DGM and ACVM identified the putative VT isthmus in 25 (89%) of the re-entrant cases. Focal activation was correctly identified by both techniques in all cases. ConclusionsDGM is a rapid automated algorithm that has a strong level of agreement with TM for manually re-annotated VT maps.

Ventricular tachycardia mechanisms and prevention in patients with severe heart failure and left ventricular assist device

Abstract Terminal Heart Failure with reduced Ejection Fraction (HFrEF) is associated with severe morbidity and mortality. Mechanical Left Ventricular Assist Devices (LVAD) are often used to provide these patients with a last resort therapy and as bridge to transplant. However, HFrEF patients with LVAD have significant myocardial substrate for ventricular arrhythmias and the LVAD itself might be regarded as pro-arrhythmogenic. Aim of the current study was to investigate the mechanism of ventricular arrhythmias in LVAD patients and to provide evidence for the hypothesis that ad-hoc ablation/substrate modification during surgical LVAD implantation might reduce the risk of VT. We retrospectively analyzed invasive ablation procedures in patients with VT±LVAD and determined the mechanism of arrhythmia during electrophysiological examination (using 3D electroanatomical and local activation time mapping; Carto; Biosense Webster) in LVAD (n=17) and non-LVAD (n=12) subgroups. Mean age of the predominantly male (97%) patients was 60±2 years. VTs were directly LVAD associated (i.e. focal, adjacent to LVAD insertion or macro-reentry, around LVAD) in almost half of the LVAD patients. Number of radiofrequency ablation (RF) lesions and RF time were not significantly different between LVAD associated VT and non-LVAD associated VT patients. Within the LVAD patient group, freedom from VT (mean follow-up 40±6 months) was 50% upon ablation in patients with VTs originating from the LVAD region and 70% if ablation was conducted in non-LVAD regions. None of the LVAD associated and 22% of non-LVAD associated VT patients died during follow-up of these critically ill patients. Moreover, to reduce LVAD related arrhythmias and based on additional ex-vivo/in-silico derived data, we propose a distinctive (i.e. “star” shaped, LVAD encirclement) epicardial substrate modification during surgical LVAD implantation. In summary, a significant percentage of patients with LVAD exhibit LVAD-associated focal/macro-reentry VT and recurrence rates are high. VT likelihood is reduced ex-vivo/in-silico upon substrate modification targeting myocardium adjacent to a possible LVAD implantation site. Epicardial RF ablation during surgical LVAD implantation might allow prevention of LVAD-associated focal/macro-reentry VT. Funding Acknowledgement Type of funding sources: Public grant(s) – National budget only. Main funding source(s): DFG

Catheter ablation of ventricular tachycardia in patients with structural heart disease

Ventricular cardiac rhythm disorders are potentially life-threatening arrhythmias. Ventricular tachycardia (VT) in patients with structural heart disease carries an increased risk of sudden cardiac death. Interventional radiofrequency catheter ablation is increasingly becoming the focus of treatment for ventricular arrhythmias. So far, no randomized study has been able to demonstrate areduction in mortality; however, depending on the existing cardiomyopathy, interventional VT ablation has proven to be more effective for rhythm stabilization than antiarrhythmic therapy and is subsequently associated with improve quality of life through reduced implantable cardioverter defibrillator (ICD) treatment. The aim of this work is to discuss the pathophysiology, mechanism and treatment of VT with structural heart disease in order to define the role of catheter ablation.

Characteristics and outcomes of ventricular tachycardia and premature ventricular contractions ablation in patients with prior mitral valve surgery.

Data regarding ventricular tachycardia (VT) or premature ventricular complex (PVC) ablation following mitral valve surgery (MVS) is limited. Catheter ablation (CA) can be challenging given perivalvular substrate in the setting of mitral annuloplasty or prosthetic valves. To investigate the characteristics, safety, and outcomes of radiofrequency CA in patients with prior MVS and ventricular arrhythmias (VA). We identified consecutive patients with prior MVS who underwent CA for VT or PVC between January 2013 and December 2018. We investigated the mechanism of arrhythmia, ablation approach, peri-operative complications, and outcomes. In our cohort, 31 patients (77% men, mean age 62.3 ± 10.8 years, left ventricular ejection fraction 39.2 ± 13.9%) with prior MVS underwent CA (16 VT; 15 PVC). Access to the left ventricle was via transseptal approach in 17 patients, and a retrograde aortic approach was used in 13 patients. A combined transseptal and retrograde aortic approach was used in one patient, and a percutaneous epicardial approach was combined with trans-septal approach in one patient. Heterogenous scar regions were present in 94% of VT patients and scar-related reentry was the dominant mechanism of VT. Forty-seven percent of PVC patients had abnormal substrate at the site targeted for ablation. Clinical VA substrates involved the peri-mitral area in six patients with VT and five patients with PVC ablation. No procedure-related complications were reported. The overall recurrence-free rate at 1-year was 72.2%; 67% in the VT group and 78% in the PVC group. No arrhythmia-related death was documented on long-term follow-up. CA of VAs can be performed safely and effectively in patients with MVS.

Structure and function of the ventricular tachycardia isthmus.

Catheter ablation of postinfarction reentrant ventricular tachycardia (VT) has received renewed interest owing to the increased availability of high-resolution electroanatomic mapping systems that can describe the VT circuits in greater detail, and the emergence and need to target noninvasive external beam radioablation. These recent advancements provide optimism for improving the clinical outcome of VT ablation in patients with postinfarction and potentially other scar-related VTs. The combination of analyses gleaned from studies in swine and canine models of postinfarction reentrant VT, and in human studies, suggests the existence of common electroanatomic properties for reentrant VT circuits. Characterizing these properties may be useful for increasing the specificity of substrate mapping techniques and for noninvasive identification to guide ablation. Herein, we describe properties of reentrant VT circuits that may assist in elucidating the mechanisms of onset and maintenance, as well as a means to localize and delineate optimal catheter ablation targets.

High density intramural mapping of post-infarct premature ventricular contractions and ventricular tachycardia.

Spontaneous ventricular premature contractions (PVCs) and ventricular tachycardia (VT) in the acute post infarct milieu is assumed to be due to automaticity. However, the mechanism has not been studied with intramural mapping. To study the mechanism of spontaneous PVCs with high density intramural mapping in a canine model, and to test the hypothesis that post-infarct PVCs and VT are due to re-entry rather than automaticity. In 15 anesthetized dogs, using 768 intramural unipolar electrograms, simultaneous recordings were made. After 20 min of stabilization, recordings were made during the first 10 min of ischemia, and activation maps of individual beats were constructed. Acute ischemia was produced by clamping the left anterior descending coronary artery proximal to the first diagonal branch. In all experiments ST-T alternans was present. Spontaneous ventricular beats occurred in five of 15 dogs where the earliest ectopic activity was manifested in the endocardium, well within the ischemic zone. From there, activity spread rapidly along the subendocardium, with endo-to epicardial spread along the non-ischemic myocardium. Epicardial breakthrough always occurred at the border of the ischemic myocardium. In three dogs, delayed potentials were observed, which were earliest at the ischemic epicardium and extended transmurally with increasing delay towards the endocardium, where they culminated in a premature beat. A similar sequence was observed in VT that followed. Graded responses that occur with each sinus beat intramurally, when able to propagate from epicardium to endocardium are the mechanism of PVCs and VT in post-infarct myocardium.

B-011-20 EVALUATION OF THE 3-DIMENSIONAL SUBSTRATE OF VENTRICULAR TACHYCARDIA IN A LANGENDORFF PERFUSED HUMAN HEART

The underlying mechanisms of ventricular tachycardia (VT) are not well understood. Most models for VT propagation are based on animal studies or single surface recordings which have limited utility. Human based investigations of VT are often limited by hemodynamic collapse and lack viable ways to assess the myocardial electrical propagation. The authors seek to provide a novel method for the experimental evaluation of VT in human hearts with correlation to high resolution MRI fibrosis imaging. Human donor hearts were obtained from discarded transplant specimens. Following explant, the hearts were cannulated to the Langendorff apparatus and ventricular tachycardia was induced using a programmed ventricular stimulation protocol. Custom built 3D printed epicardial and endocardial mapping probes were deployed to map whole ventricular contraction. The hearts were imaged using high-resolution late gadolinium enhancement 4T MRI for fibrosis quantitation. A total of 8 human hearts underwent complete mapping procedures with 3 spontaneously beating VT hearts and 5 control hearts. High resolution mapping demonstrated VT originated from epicardial regions in all 3 hearts. Site of origin of VT was identified in all 3 human hearts and correlated to MRI fibrosis mapping. This study highlights new methods for the interrogation of ventricular tachycardia substrates using a novel human Langendorff heart model. The integration of mapping and imaging techniques in this study provides new insights into the mechanisms underlying VT. These efforts may help clinicians to provide more targeted ablation procedures.

Updates in Ventricular Tachycardia Ablation.

Sudden cardiac death (SCD) due to recurrent ventricular tachycardia is an important clinical sequela in patients with structural heart disease. As a result, ventricular tachycardia (VT) has emerged as a major clinical and public health problem. The mechanism of VT is predominantly mediated by re-entry in the presence of arrhythmogenic substrate (scar), though focal mechanisms are also important. Catheter ablation for VT, when compared to standard medical therapy, has been shown to improve VT-free survival and burden of device therapies. Approaches to VT ablation are dependent on the underlying disease process, broadly classified into idiopathic (no structural heart disease) or structural heart disease (ischemic or non-ischemic heart disease). This update aims to review recent advances made for the treatment of VT ablation, with respect to current clinical trials, peri-procedure risk assessments, pre-procedural cardiac imaging, electro-anatomic mapping and advances in catheter and non-catheter based ablation techniques.

Focal Ventricular Tachycardias in Structural Heart Disease: Prevalence, Characteristics, and Clinical Outcomes After Catheter Ablation.

This study sought to summarize the procedural characteristics and outcomes of patients with structural heart disease (SHD) who have focal ventricular tachycardia (VT). Scar-mediated re-entry is the predominant mechanism of VT in SHD. Some SHD patients may have a focal VT mechanism that remains poorly described. An extended induction protocol incorporating programmed electrical stimulation, right ventricular burst pacing and isoprenaline was used to elucidate both re-entrant and focal VT mechanisms. Eighteen of 112 patients (16%) with SHD undergoing VT ablation over 2 years had a focal VT mechanism elucidated (mean age 66±13 years; ejection fraction 46±14%; nonischemic cardiomyopathy 10). Repetitive failure of termination with antitachycardia pacing (ATP) (69% of patients) or defibrillator shocks (56%) was a common feature of focal VTs. A median of 3 VTs per patient were inducible (28 focal VTs, 34 re-entrant VTs; 53% of patients had both focal and re-entrant VT mechanism). Focal VTs more commonly originated from the right ventricle (RV) than the left ventricle (LV) (67% vs. 33%, respectively). In the RV, the RV outflow tract was the most common site (33% of all focal VTs), followed by the RV moderator band (22%), apical septal RV (6%), and lateral tricuspid annulus (6%). The lateral LV (non-Purkinje) was the most common LV focal VT site (16%), followed by the papillary muscles (17%). After median follow-up of 289 days, 78% of patients remained arrhythmia-free; no patients had recurrence of focal VT at repeat procedure. In patients with recurrence, defibrillator therapies were significantly reduced from a median of 53 ATP episodes pre-ablation to 10 ATP episodes post-ablation. During follow-up, 2 patients (11%) underwent repeat VT ablation; none had recurrence of focal VT. Focal VTs are common in patients with SHD and often coexist with re-entrant forms of VT. High failure rate of defibrillator therapies was a common feature of focal VT mechanisms. Uncovering and abolishing focal VT may further improve outcomes of catheter ablation in SHD.

Cardiovascular Magnetic Resonance-Based Three-Dimensional Structural Modeling and Heterogeneous Tissue Channel Detection in Ventricular Arrhythmia

Geometrical structure of the myocardium plays an important role in understanding the generation of arrhythmias. In particular, a heterogeneous tissue (HT) channel defined in cardiovascular magnetic resonance (CMR) has been suggested to correlate with conduction channels defined in electroanatomic mapping in ventricular tachycardia (VT). Despite the potential of CMR for characterization of the arrhythmogenic substrate, there is currently no standard approach to identify potential conduction channels. Therefore, we sought to develop a workflow to identify HT channel based on the structural 3D modeling of the viable myocardium within areas of dense scar. We focus on macro-level HT channel detection in this work. The proposed technique was tested in high-resolution ex-vivo CMR images in 20 post-infarct swine models who underwent an electrophysiology study for VT inducibility. HT channel was detected in 15 animals with inducible VT, whereas it was only detected in 1 out of 5 animal with non-inducible VT (P < 0.01, Fisher’s exact test). The HT channel detected in the non-inducible animal was shorter than those detected in animals with inducible VTs (inducible-VT animals: 35 ± 14 mm vs. non-inducible VT animal: 9.94 mm). Electrophysiology study and histopathological analyses validated the detected HT channels. The proposed technique may provide new insights for understanding the macro-level VT mechanism.

Long term follow-up after ventricular tachycardia ablation in patients with congenital heart disease.

Ventricular tachycardia (VT) is frequently encountered in patients with repaired and unrepaired congenital heart disease (CHD), causing significant morbidity and sudden cardiac death. Data regarding underlying VT mechanisms and optimal ablation strategies in these patients remain limited. To describe the electrophysiologic mechanisms, ablation strategies, and long-term outcomes in patients with CHD undergoing VT ablation. Forty-eight patients (mean age 41.3 ± 13.3 years, 77.1% male) with CHD underwent a total of 57 VT ablation procedures at two centers from 2000 to 2017. Electrophysiologic and follow-up data were analyzed. Of the 77 different VTs induced at initial or repeat ablation, the underlying mechanism in 62 (81.0%) was due to scar-related re-entry; the remaining included four His-Purkinje system-related macrore-entry VTs and focal VTs mainly originating from the outflow tract region (8 of 11, 72.7%). VT-free survival after a single procedure was 72.9% (35 of 48) at a median follow-up of 53 months. VT-free survival after multiple procedures was 85.4% (41 of 48) at a median follow-up of 52 months. There were no major complications. Three patients died during the follow-up period from nonarrhythmic causes, including heart failure and cardiac surgery complication. While scar-related re-entry is the most common VT mechanism in patients with CHD, importantly, nonscar-related VT may also be present. In experienced tertiary care centers, ablation of both scar-related and nonscar-related VT in patients with CHD is safe, feasible, and effective over long-term follow-up.

Interdigitating Myocardial Tongues in Pediatric Cardiac Fibromas: Plausible Substrate for Ventricular Tachycardia and CardiacArrest.

This study sought to evaluate for the presence of and characterize the interdigitating and entrapped myocardium within cardiac fibromas (CF) and correlate tissue findings with symptoms and surgical outcomes. The mechanism of ventricular tachycardia (VT) in CF is unclear. The authors hypothesized that CF harbor tongues of interdigitating myocardium, which could be a substrate for episodes of arrhythmia analogous to peri-infarct zones. A total of 29 patients (14 boys) with CF were identified; all subjects had undergone at least partial tumorresection. A semiquantitative grading system was used to assess the degree of myocardial interdigitation and entrapment, myocyte morphology (hematoxylin and eosin stain and immunohistochemical stain for desmin), tumor collagen density, and cellularity (trichrome stain). The subjects' ages at presentation, types of arrhythmia, and responses to surgery were correlated with histology. CF consistently demonstrated interdigitating and entrapped myocardium, and the extent correlated negatively with age at surgery, as did cellularity, whereas collagen increased with age. Median age at arrhythmia recognition was 8 months. Sustained VT was present in 18 of 29 patients (62%), and 5 of 6 patients with prenatally diagnosed conditions developed VT before 8 months. All 8 patients who experienced cardiac arrest had clinically significant arrhythmia events. Sustained arrhythmia episodes correlated with more diffuse myocyte interdigitation. Ten patients hadabnormal karyotype: chromosomes 9 (n= 3) and 3 (n= 1) deletions; isolated translocations: t(4;13), t(5;11) and t(1;9); andundefined aberrations (n= 3). All patients who underwent complete resection were cured of arrhythmias, whereas 2of 14 patients who had subtotal resections had recurrence, with resolution following re-resection in 1 patient. Interdigitating myocardium represents a potential histopathologic substrate for VT and cardiac arrestin CF, which may also explain the occasional recurrence of arrhythmia following incomplete resection.